NEUROPROTECTIVE EFFECT OF c-fos ANTISENSE OLIGODEOXYNUCLEOTIDE UPON APOPTOSIS INDUCED BY SODIUM SELENITE IN CULTURED CORTICAL NEURONS: POSSIBLE CASCADE OF ACTIVATION OF RELATED GENES
- VernacularTitle:c-fos反义寡聚核苷酸对亚硒酸钠引起的皮质神经元凋亡的保护作用
- Author:
Rong XIAO
;
Yan DOU
;
Jiahui ZHAO
;
Rui WANG
;
Xiuzhen YAN
;
Jiantian QIAO
- Publication Type:Journal Article
- Keywords:
apoptosis;
sodium selenite;
antisense oligodeoxynucleotide;
c-fos;
cultured cortical neurons;
newborn mice
- From:
Chinese Journal of Neuroanatomy
2002;18(2):93-100
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the role of immediate-early gene c-fos in sodium selenite-induced apoptosis and its position in a possible cascade of apoptogenic genes, we compared the time-courses of expression for 5 related genes, including c-fos, during the apop- tosis induced by sodium selenite with or without blockage of c-fos expression by adding c-fos antisense oligodeoxynucleotide ( ASO) in cultured cortical neurons. The results showed that: (1) in control experiments without c-fos ASO adding, 0. 5 μmol/ L sodium selenite-induced apoptosis as revealed by electrophoretic and flow cytometric examinations; at the same time, sodium selenite also induced down-regulation of bcl-2 mRNA expression and up-regulations of mRNAs related to bax, c-fos, p53, and acetylcholinesterase (AChE) genes; (2) in similar experimental conditions with c-fos ASO cotreatment, the sodium selenite-in- duced apoptosis was blocked with the up-regulation of p53 expression still emerging as before, while the changes in expressions of bcl-2, bax, AChE genes were reversed at the same time. The results suggest that c-fos ASO could play a protective role upon cortical neurons from suffering apoptosis induced by sodium selenite, and there might exist a cascade of gene expressions with p53 and c-fos genes being regulated upstream and then bcl-2, bax, and AChE genes being regulated downstream.
